Before Darwin - Some believe organisms gradually wear out and deteriorate in
the same manner as non-living things

Before Darwin - No evidence that origin
of life span different from any other organism characteristic that differs
between species, i.e. organisms appear to be designed to have a species-specific
life span

1859+ - Darwin?s critics note the contradiction between the Darwinian concept of natural selection favoring
individuals with maximal survival and reproductive capacity and the observed progressive decline of vital and reproductive capacities, i.e.
a limited life span that differed greatly between similar species (see Goldsmith 2004)

1859+ - Darwin suggests that a limited life span must convey some unknown benefit that offset its otherwise
adverse effect. He did not specify the nature of the benefit. (see Goldsmith 2004)

1889 - Weismann hints that the death of old individuals was beneficial because this gave more space
to new generations and that this was useful for the evolution of species (Weismann 1889;
see Kirkwood & Cremer 1982)

1889 - Weismann observes that the cells of the various organs and tissues are renewed continuously and that when this
turnover slackens or stops, the organs or the tissues reduce or lose their functionality with negative effects on fitness
(see Kirkwood & Cremer 1982)

1983+ - The final incapability of a cell to duplicate (replicative senescence) is shown to be not an abrupt
event but a progressive reduction of cell duplication potential which depends on the reduction of telomere length
(Pontèn et al. 1983; Jones et al. 1985)

1997+ - "Proapoptosis" (Hochman 1997), a form of eubacterial cell suicide, is shown
to be clearly related to eukaryotic apoptosis (Koonin & Aravind 2002) and
this indicates a very old evolutionary persistence and similarity

1999 - The death of an individual, when not determined by accidents or diseases and as event
provoked by particular mechanisms genetically regulated, namely programmed, and therefore somehow
favoured by natural selection, is defined for the first time by a specific neologism,
"phenoptosis" (Skulachev 1999)

2005 - Cell senescence is defined as a "fundamental cellular program"
(Ben-Porath & Weinberg 2005)
as the changes that define it are stereotyped and predictable. Replicative senescence is part of cell senescence
phenomenon. The degree of senescence of a culture is determined by the fraction of cells in cell senescence state.

2009 - Evolutionary classification of diseases and of disease-like phenomena (as aging). Definition of a research
program to master aging with the modification of its physiological mechanisms
(Libertini 2009b)

2010 - Strong empirical and theoretical arguments in support of ageing adaptive theories:
"Several lines of evidence suggest that [telomere-cell senescence system] was selected first and foremost
to cause ageing" (Milewski 2010)

2011 - For the first time, Kirkwood, an authoritative supporter of non-adaptive hypotheses about ageing, admits that “ageing might occasionally be adaptive” (Kirkwood & Melov 2011)

2011 - For the first time, it is proposed a phylogeny of the age-related fitness decline (alias mortality increase) – a phenomenon generally referred imprecisely “aging” – and of related phenomena (Libertini 2011)

2011 - Human senescent and centenarian cells are transformed into pluripotent stem cells with reset telomere size, gene expression profiles, oxidative stress, and mitochondrial metabolism, which are indistinguishable from young embryonic stem cells (Lapasset et al. 2011). This is another experiment proving how cell senescent state is not an irreversible condition caused by the accumulation of “errors” or toxic substances, but a physiologic state that is entirely reversible by an opportune reprogramming.

2012 - Special issue of the journal Biochemistry (Moscow), directed by V. Skulachev, exclusively about Phenoptosis phenomenon (Vol. 77, n. 7). For the first time in an academic journal, vertebrate aging is correctly framed within phenomena of programmed death, alias phenoptosis.